File download Interface MALDI-IMS(병리학회발표) ver1
Breast cancer is one of the most common female cancers and known to metastasize to brain. It is acknowledged that brain prevents the entering of substances in the blood stream by blood-brain barrier (BBB) and only tiny materials can across the BBB. In terms of size, cancer cells are too large to penetrate the BBB. However, 30% of all women with metastatic breast cancer develop brain tumors. Recently, many studies have suggested that the reciprocal interaction between cancer cells and environment is important for cancer metastasis. Therefore, it is plausible that tumor microenvironment is involved in breast cancer brain metastasis. Our research is to understand the role of Interface Zone in breast cancer brain metastasis.
CSCs resemble cells that have undergone epithelial–mesenchymal transition (EMT) with regard to their invasiveness and motility. EMT, which is associated with a key step in tumor metastasis via induction of a highly invasive phenotype, has been intensely studied. And CSCs have been found to transiently acquire stem cell-like properties as a consequence of EMT. CSCs also are inherently chemoresistant and radioresistant. Recently, side population (SP) cells have been shown to express increased levels of MDR1 (multidrugresistance protein 1) and ABCG2 (ATP-binding cassette, sub-family G, member 2) transporters, which can extrude certain chemotherapeutic agents and have been implicated in drug resistance. Importantly, SP cells appear to be enriched in stem cells. Although this issue remains controversial, identifying and characterizing human ovarian CSCs would provide a critical step toward the identification of drugs with therapeutic efficacy against CSCs and the development of novel therapeutic strategies for the long-term control of cancer.
Contemporary issue
– Balance score of pro-(MCP-1, IL-6, MMP) and anti-malignant (IP-10) factors: 1.36~ 2.44 (Witz, IJCa 2003)
– No MECE
– TNF family
Proinflammatory cytokine as promalignant effect (since R. Virchow, 1863)
– TGF-β
> Inhibit normal mammary epithelail cells
> Enhance tumor cell invasion/mets:
– loss of anti-proliferative role
– mutation in TGFBR
– inhibition of SMAD pathway
– suppressing anti-tumor immune response
– augmenting angiogenesis